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Epstein-Barr virus (EBV) is known to be associated with several malignancies. This virus has tropism for B lymphocytes and is capable of establishing latency programs that alter the maturation pathway of these lymphocytes to persist latently in memory B cells. During its latency programs, EBV expresses viral proteins such as LMP-1 and LMP-2a, which prevent apoptosis and promote differentiation of the infected cell. These viral proteins are oncogenic and allow the survival of B lymphocytes with malignant mutations. The ontogeny of B lymphocytes includes highly mutagenic processes such as: V(D)J recombination, somatic hypermutation (SMH) and class switch recombination (CSR). In this review, we will describe basic aspects of the EBV life cycle and the maturation process of B lymphocytes leading to the formation of antibody-producing plasma cells or memory B cells. The aim of this review is to understand how these two events are highly interrelated and how their intersection increases the risk of lymphoma development. A better understanding of the interaction between EBV and the B cell ontogeny may contribute to the development of new therapeutic, diagnostic or preventive strategies. [ABSTRACT FROM AUTHOR]